A cross-country comparison of math achievement at teen age and cognitive performance 40 years later

BACKGROUND Maintaining cognitive functioning through mid- to late-life is relevant for the individual and societal aim of active ageing. Evidence shows considerable stability in individual-level rank-ordering of cognitive functioning, but little attention has been given to cohort performance over the life cycle and macro-level factors that could affect it. OBJECTIVE The main goal of this paper is to address cross-national variation in mental performance from younger to older ages. METHODS Using a quasi-longitudinal approach, we compare the relative country ranking in standardised mathematical test scores of young teenagers in 1964 from the First International Mathematics Study (FIMS) and cognitive test performance at mid-life in 2004, based on the Survey of Health, Ageing and Retirement in Europe(SHARE) for the cohort born between 1949 and 1952. RESULTS Our results show that those countries which had the highest scores in math tests taken by 13-year-old-grade-level students are not the same countries that, 40 years later, have the top performing scores in cognitive tests among mid-age adults. CONCLUSIONS This article highlights the importance of considering country-level influences on cognitive change over the life cycle, in addition to individual characteristics, and provides some descriptive findings that could be incorporated with further research on the link between specific contextual factors and cognitive functioning

High-Temperature Short-Time Treatment of Human Milk for Bacterial Count Reduction

Background: Human milk (HM) for preterm infants will often be pasteurized for cytomegalovirus (CMV) inactivation and reduction of its bacterial count. High-temperature short-time (HTST) treatment compared to standard Holder pasteurization (HoP) reduces the impact of heat treatment on bioactive HM proteins while effectively inactivating CMV. No data are available for the efficacy of bacterial count reduction using HTST treatments that are available for clinical use.Objective: To test the antiviral and antibacterial efficacy of HTST treatment protocols in HM using a modified HTST treatment device compared to standard HoP.Methods: Holder pasteurized 95 mL HM samples were inoculated with Staphylococcus aureus (ATCC 6538), Enterococcus faecalis (ATCC 29212), Pseudomonas aeruginosa (ATCC 27853), Serratia marcescens (Smarc 00697), two different strains of Klebsiella pneumoniae (ATCC 700603 and Kpn 01605) or spiked with 2 × 105 50% tissue culture infective dose of CMV (AD169) and subsequently subjected to HoP (62.5°C/30 min) or HTST treatment (62°C/5 s, 62°C/15 s, 72°C/5 s, 72°C/15 s, 87°C/2 s, and 87°C/5 s). Bacterial count was determined after treated HM was cultured for 24 h. CMV infectivity was determined by the number of specific CMV immediate early antigen stained nuclei after inoculating human fibroblasts with appropriately prepared HM samples.Results: Holder pasteurized samples revealed no growth after 24 h incubation. Viable bacterial cultures were retrieved from all tested strains after HTST treatment with the default HTST protocol (62°C/5 s) that is available for clinical use. Using other time-temperature combinations, growth rates of S. aureus, E. faecalis, P. aeruginosa, K. pneumoniae, K. pneumonia, and S. marcescens were depending on treatment time, treatment temperature, bacterial genera and strain. Only after treatment temperatures above 72°C no bacterial growth was observed. CMV was inactivated by any tested time-temperature combination.Conclusions: HTST treatment inactivates CMV in 95 mL HM samples but is less effective than HoP in bacterial count reduction at a time-temperature combination of 62°C/5 s. For a reliable bacterial count reduction HTST treatment at 87°C was required in this study

BIOFILMS AND THE PATHOGENESIS OF THE APICAL PERIODONTITIS

O controle de uma infecção endodôntica demanda um esforço concentrado de fatores gerais do hospedeiro e de medidas de tratamento a partir da compreensão da etiologia e patogênese das doenças endodônticas. Atualmente há uma tendência de se considerar as lesões perirradiculares como doença induzida por biofilme. Este artigo de revisão tem como objetivo apresentar o biofilme dentro do conceito de comunidade como unidade de patogenicidade. O conhecimento e a compreensão do conceito de comunidade são importantes, pois o aprimoramento do endodontista no campo da microbiologia é fundamental para o entendimento do processo infeccioso que se propõe a eliminar. Isto se justifica para poder elaborar estratégias que permitam tratar de forma previsível o dente acometido.[Vieira MVB, Moreno JO, Lopes WSP, Martínez AM. Biofilme e a patogênese das lesões perriradiculares. Ustasalud 2011; 10: 60 - 64]The control of an endodontic infection requires a concerted effort of general host factors and treatment measures based upon the understanding of the etiology and pathogenesis of endodontic diseases. Currently there is a tendency to consider apical periodontitis as a disease induced by biofilm. This review aims to present the biofilm within the concept of community as the unit of pathogenicity. Knowledge and understanding of the concept of community is important, because improving the endodontist in the field of microbiology is essential for a better understanding of the infectious process to be eliminated

The Psychologist in Child Education: A Proposal for Psychosocial Intervention

This research aimed to share an experience of psychosocial intervention developed by students and professionals of school psychology within an Early Childhood Education public institution located in the city of Campinas, through a project called The Eagle’s Flight. The main activities developed by the psychology team at this institution were: (1) School and social mapping of life; (2) Life and Schooling Trajectories follow up; (3) Participation in Teacher Training meetings; (4) Weaving intersectoral networks; (5) Meeting with family; and, (6) Strengthening of academic and professional training. In general, the Eagle´s Flight project allowed to stay in touch with a population that has its basic rights denied in a daily basis, which drove in the team the need to develop interventions that mobilized subjects to change their social conditions. For this, was developed a practice directed to the process of process of awareness, strengthening and coping with adverse conditions of everyday lif

ETS-related gene (ERG) undermines genome stability in mouse prostate progenitors via Gsk3β dependent Nkx3.1 degradation.

21q22.2-3 deletion is the most common copy number alteration in prostate cancer (PCa). The genomic rearrangement results in the androgen-dependent de novo expression of ETS-related gene (ERG) in prostate cancer cells, a condition promoting tumor progression to advanced stages of the disease. Interestingly, ERG expression characterizes 5-30% of tumor precursor lesions - High Grade Prostatic Intraepithelial Neoplasia (HGPIN) - where its role remains unclear. Here, by combining organoids technology with Click-chemistry coupled Mass Spectrometry, we demonstrate a prominent role of ERG in remodeling the protein secretome of prostate progenitors. Functionally, by lowering autocrine Wnt-4 signaling, ERG represses canonical Wnt pathway in prostate progenitors, and, in turn, promotes the accumulation of DNA double strand breaks via Gsk3β-dependent degradation of the tumor suppressor Nkx3.1. On the other hand, by shaping extracellular paracrine signals, ERG strengthens the pro-oxidative transcriptional signature of inflammatory macrophages, which we demonstrate to infiltrate pre-malignant ERG positive prostate lesions. These findings highlight previously unrecognized functions of ERG in undermining adult prostate progenitor niche through cell autonomous and non-autonomous mechanisms. Overall, by supporting the survival and proliferation of prostate progenitors in the absence of growth stimuli and promoting the accumulation of DNA damage through destabilization of Nkx3.1, ERG could orchestrate the prelude to neoplastic transformation

Body shape phenotypes of multiple anthropometric traits and cancer risk: a multi-national cohort study

Background - Classical anthropometric traits may fail to fully represent the relationship of weight, adiposity, and height with cancer risk. We investigated the associations of body shape phenotypes with the risk of overall and site-specific cancers. Methods - We derived four distinct body shape phenotypes from principal component (PC) analysis on height, weight, body mass index (BMI), waist (WC) and hip circumferences (HC), and waist-to-hip ratio (WHR). The study included 340,152 men and women from 9 European countries, aged mostly 35–65 years at recruitment (1990–2000) in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Cox proportional hazards regression was used to estimate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs). Results - After a median follow-up of 15.3 years, 47,110 incident cancer cases were recorded. PC1 (overall adiposity) was positively associated with the risk of overall cancer, with a HR per 1 standard deviation (SD) increment equal to 1.07 (95% confidence interval 1.05 to 1.08). Positive associations were observed with 10 cancer types, with HRs (per 1 SD) ranging from 1.36 (1.30–1.42) for endometrial cancer to 1.08 (1.03–1.13) for rectal cancer. PC2 (tall stature with low WHR) was positively associated with the risk of overall cancer (1.03; 1.02–1.04) and five cancer types which were not associated with PC1. PC3 (tall stature with high WHR) was positively associated with the risk of overall cancer (1.04; 1.03–1.05) and 12 cancer types. PC4 (high BMI and weight with low WC and HC) was not associated with overall risk of cancer (1.00; 0.99–1.01). Conclusions - In this multi-national study, distinct body shape phenotypes were positively associated with the incidence of 17 different cancers and overall cancer

Visceral adipose tissue immune homeostasis is regulated by the crosstalk between adipocytes and dendritic cell subsets

Visceral adipose tissue (VAT) has multiple roles in orchestrating whole-body energy homeostasis. In addition, VAT is now considered an immune site harboring an array of innate and adaptive immune cells with a direct role in immune surveillance and host defense. We report that conventional dendritic cells (cDCs) in VAT acquire a tolerogenic phenotype through upregulation of pathways involved in adipocyte differentiation. While activation of the Wnt/β-catenin pathway in cDC1 DCs induces IL-10 production, upregulation of the PPARγ pathway in cDC2 DCs directly suppresses their activation. Combined, they promote an anti-inflammatory milieu in vivo delaying the onset of obesity-induced chronic inflammation and insulin resistance. Under long-term over-nutrition, changes in adipocyte biology curtail β-catenin and PPARγ activation, contributing to VAT inflammation

Deletion of Fibroblast Growth Factor Receptor 2 from the Peri-Wolffian Duct Stroma Leads to Ureteric Induction Abnormalities and Vesicoureteral Reflux

Purpose: Pax3cre-mediated deletion of fibroblast growth factor receptor 2 (Fgfr2) broadly in renal and urinary tract mesenchyme led to ureteric bud (UB) induction defects and vesicoureteral reflux (VUR), although the mechanisms were unclear. Here, we investigated whether Fgfr2 acts specifically in peri-Wolffian duct stroma (ST) to regulate UB induction and development of VUR and the mechanisms of Fgfr2 activity. Methods: We conditionally deleted Fgfr2 in ST (Fgfr2 ST-/- ) using Tbx18cre mice. To look for ureteric bud induction defects in young embryos, we assessed length and apoptosis of common nephric ducts (CNDs). We performed 3D reconstructions and histological analyses of urinary tracts of embryos and postnatal mice and cystograms in postnatal mice to test for VUR. We performed in situ hybridization and real-time PCR in young embryos to determine mechanisms underlying UB induction defects. Results: We confirmed that Fgfr2 is expressed in ST and that Fgfr2 was efficiently deleted in this tissue in Fgfr2 ST-/- mice at embryonic day (E) 10.5. E11.5 Fgfr2 ST-/- mice had randomized UB induction sites with approximately 1/3 arising too high and 1/3 too low from the Wolffian duct; however, apoptosis was unaltered in E12.5 mutant CNDs. While ureters were histologically normal, E15.5 Fgfr2 ST-/- mice exhibit improper ureteral insertion sites into the bladder, consistent with the ureteric induction defects. While ureter and bladder histology appeared normal, postnatal day (P) 1 mutants had high rates of VUR versus controls (75% versus 3%, p = 0.001) and occasionally other defects including renal hypoplasia and duplex systems. P1 mutant mice also had improper ureteral bladder insertion sites and shortened intravesicular tunnel lengths that correlated with VUR. E10.5 Fgfr2 ST-/- mice had decreases in Bmp4 mRNA in stromal tissues, suggesting a mechanism underlying the ureteric induction and VUR phenotypes. Conclusion: Mutations in FGFR2 could possibly cause VUR in humans. © 2013 Walker et al

Blockade of interleukin-6 signalling with siltuximab enhances melphalan cytotoxicity in preclinical models of multiple myeloma

Signalling through the interleukin (IL)-6 pathway induces proliferation and drug resistance of multiple myeloma cells. We therefore sought to determine whether the IL-6-neutralizing monoclonal antibody siltuximab, formerly CNTO 328, could enhance the activity of melphalan, and to examine some of the mechanisms underlying this interaction. Siltuximab increased the cytotoxicity of melphalan in KAS-6/1, INA-6, ANBL-6, and RPMI 8226 human myeloma cell lines (HMCLs) in an additive-to-synergistic manner, and sensitized resistant RPMI 8226.LR5 cells to melphalan. These anti-proliferative effects were accompanied by enhanced activation of drug-specific apoptosis in HMCLs grown in suspension, and in HMCLs co-cultured with a human-derived stromal cell line. Siltuximab with melphalan enhanced activation of caspase-8, caspase-9, and the downstream effector caspase-3 compared with either of the single agents. This increased induction of cell death occurred in association with enhanced Bak activation. Neutralization of IL-6 also suppressed signalling through the phosphoinositide 3-kinase/Akt pathway, as evidenced by decreased phosphorylation of Akt, p70 S6 kinase and 4E-BP1. Importantly, the siltuximab/melphalan regimen demonstrated enhanced anti-proliferative effects against primary plasma cells derived from patients with myeloma, monoclonal gammopathy of undetermined significance, and amyloidosis. These studies provide a rationale for translation of siltuximab into the clinic in combination with melphalan-based therapies